Respiratory viral infections in children with asthma: do they matter and can we prevent them?

Ahanchian, Hamid; Jones, Carmen M; Chen, Yueh-sheng; Sly, Peter D

As discussed above, evidence exists for an impaired innate immune response to respiratory viral infections in asthmatics [141] . Entry of rhinovirus into normal epithelial cells initiates a vigorous innate immune response with IFN-β secretion and apoptosis induction. In asthma, IFN-β and IFN-λ responses are impaired, resulting in viral replication, cell cytotoxicity, enhanced virion shedding and increased susceptibility to common cold [17, 142] . Epithelial cells of asthmatic patients responded to exogenous treatment with IFN-β exhibiting reduced rhinovirus release (Cakebread, Xu et al. 2011; Jackson, Sykes et al. 2011). If the proposed deficiency of type I and III contribute to asthma exacerbations [21, 22, 143] , correcting this deficiency with exogenous interferons would be a logical approach. The advantages of interferon application include the broad spectrum of activity with low risk of resistance development [47] . Prophylactic intranasal recombinant IFN-α and IFN-β have been shown to be effective against rhinovirus infection in humans [144] [145] [146] . The results of these clinical trials are awaited with interest [147, 148] . However, the systemic symptoms associated with severe viral infections, e.g. influenza, are associated with interferons, so careful dosing may be required. Considering the occurrence of the local side effects, neutropenia and cost, the use of long-term prophylaxis with daily, intranasal administration of interferons is not feasible [144] . However, randomized clinical trials using similar strategies are currently underway in adults with chronic respiratory disease and the results are keenly awaited.